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Y3/ Pathology > Healing and Repair > Flashcards

Healing and Repair Flashcards

1
Q

What things cause tissue injury?

A 
surgical 
infection 
burns
inflammation 
ischaemia 
toxins 
trauma
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2
Q

What three things does healing depend on?

A
  1. the type of tissue that is injured
  2. the nature of the injury
  3. sufficient blood supply (angiogenesis)
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3
Q

Describe the layers of the skin

A
  • epidermis = contains stem cells in constant cell cycle
  • dermo-epidermal junction = connects epidermis to dermis via hemidesmosomes, basement membrane and collagen
  • dermis = comprises fibroblasts, blood vessels and abundant ECM
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4
Q

What is the ECM of the dermis comprised of?

A
  • collagen fibres - provide structural support
  • proteoglycans - form a hydrated gel which resist compressive forces whilst permitting rapid diffusion of nutrients, metabolite and hormones
  • elastic fibres - provide resilience by stretch and recoil functions
  • basement membrane
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5
Q

What is the basement membrane made up of?

A
  • laminin
  • Type IV collagen
  • plasma membrane
  • perlecan
  • nitrogen
  • integrin = main receptor type by which cells bind to ECM, anchors to BM
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6
Q

What is the different between wound healing by primary and secondary intention?

A

Primary intention = when the wound edges of the epidermis can be brought close together.
Secondary intention = wound edges far apart, gap fills in by granulation tissue,

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7
Q

What are the phases of wound healing?

A
  • clotting
  • granulation tissue
  • angiogenesis
  • fibroplasia
  • re-epithelialisation
  • wound contraction and scarring
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8
Q

Describe the clotting phase

A

fibrin clot provides rapid structural support following injury

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9
Q

Describe the granulation tissue phase

A

the ‘provisional ECM’

  • inflammatory cells blood vessels, fibroblasts, loose fibrous tissue
  • will not support epithelial layer until angiogenesis and fibroplasia have taken place
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10
Q

Describe the angiogenic phase

A
  • proteolysis of ECM
  • migration and chemotaxis
  • proliferation of endothelial cells
  • lumen formatin, maturation and inhibition of growth
  • increased permeability through gaps and transcytosis
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11
Q

Describe fibroplasia

A
  • fibroblast proliferation and migration
  • production of collagen, proteoglycans and elastic to re-form the ECM
  • few inflammatory cells now
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12
Q

Describe re-epithelialisation

A
  • keratinocyte migration from edge of wound and skin appendages begins within 24hrs of injury
  • keratinocyte proliferation is inhibited until migration is complete
  • depends upon re-establishment of the derma-epidermal junction
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13
Q

Describe wound contraction and scarring

A
  • complete re-epithelialisation and dermal scarring
  • note the parallel orientation of collagen fibres and the more densely cellular dermis (normally random organisation)
  • fibroblasts develop properties of SM cells (myofibroblasts) allowing contraction of the wound
  • some residual inflammation is present
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14
Q

Describe the regulation of wound healing in skin

A
  • macrophages, fibroblasts and endothelial cells produce growth factors which stimulate healing in epidermis and dermis
  • integrins are major receptors of ECM and initiate growth factors signalling pathways
  • MMPs are unregulated leading to remodelling of ECM, MMPs are inhibited by TIMPs (tissue inhibitor metalloproteases)
  • regulated by growth factors, importantly TGF-beta
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15
Q

What systemic and local factors influence wound healing?

A 
Systemic 
- nutrition 
- metabolic status 
- circulatory status 
- hormones 
Local 
- local blood supply 
- infection 
- foreign body 
- mechanical factors
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16
Q

What is the wound strength at 1 week, w month and 3 months?

A

1 week = 10%
2 months = 50-60%
3 months = 70-80% –> plateau (collagen is deposited)

17
Q

Give 3 examples of pathological healing of skin

A

Keloid scarring
- normally in pigmented skin, hypertrophic collagen fibres,
Contractures
- following injury over a large surface e.g. burns
Chronic leg ulcer
- no healing especially in PVD or diabetes as insufficient blood supply and nutrients for healing

18
Q

Describe the location and appearance of ECM in the liver

A
  • ECM is predominately confined to the portal tracts with only a thin layer in contact with hepatocytes, composed mainly of collagen (reticulin)
19
Q

Describe regeneration of the liver following injury

A
  • hepatocytes stimulated out of ‘quiescent’ G0 phase back into cell cycle
  • new ECM is deposited between hepatocytes
  • angiogenesis establishes new sinusoids
20
Q

What is the difference between resolution and repair in the liver?

A 
Resolution = regrowth to normal tissue 
Repair = e.g. cirrhosis, repaired structured are not normal
21
Q

Describe the regulation of liver healing/fibrosis

A
  • stellate and Kupferr cells produce growth factors and cytokines which stimulate healing
  • hepatocyte growth factor (HGF) plays a key role in stimulating hepatocytes to enter cell cycle
  • TGF-beta is one of the key regulators of fibrosis
  • as in skin, the deposited collagen is remodelled by MMPs and TIMPs
22
Q

What factors affect the development of cirrhosis?

A

Time cours of liver injury
- paracetamol overdose causes severe liver injury at one point in time - does not lead to cirrhosis
- alcohol generally causes much less severe injury but over a longer time period - can cause cirrhosis
Anatomic site of injury
- damage to parenchyma (e.g. alcohol) causes classical cirrhosis with fibrosis mediated largely by stellate cells in the sinusoids
- damage to portal tracts (e.g. primary biliary cholangitis) causes a biliary pattern of fibrosis mainly affecting the portal structures

23
Q

What are the clinical consequences of cirrhosis?

A
  • jaundice
  • spider naevi, palmer erythema, gynaecomastia, splenomegaly, flapping tremor
  • loss of parenchymal function: impaired protein synthesis, processing drugs and hormones and production of clotting factors
  • portal hypertension
  • infection (spontaneous bacterial peritonitis)
  • hepatocellar carcinoma
24
Q

Describe the regulation of fibrosis in myocardial infarction

A
  • fribroblasts and myofibroblasts produce matrix proteins in response to inflammatory mediates released by macrophages and inflammatory cells
  • mediators of fibrosis include inflammatory cytokines such as TNF-alpha, IL-1, IL-6 and fibrogenic factors such as TGF-beta, PDGF and angiotensin II
25
Q

What are the consequences of myocardial fibrosis?

A
  • contractile dysfunction
  • arrhythmia
  • myocardial rupture
  • pericarditis
  • ventricular aneurysm
  • papillary muscle dysfunction
26
Q

What are labile cells?

Give 4 examples

A

Labile cells = can regrow

  • haemopoietic cells
  • squamous epithelium
  • columnar epithelium
  • urothelium
27
Q

What are stable cells?

Give 5 examples

A

Stable cells = normally in G0 but do have the ability to regrow

  • hepatocytes
  • pancreatic acinar cells
  • fibroblasts
  • smooth muscle
  • endothelium
28
Q

What are permanent cells?

Give 3 examples

A

Permanent cells = low capacity to divide

  • cardiac myocytes
  • neurones
  • skeletal muscle

Y3/ Pathology (15 decks)

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